Satiety signalling: difference between revisions
Diff·revision 17 → 18·21:10, 10 Aug 2025
Difference between revision 17 and revision 18 of Satiety signalling. 2 lines changed; the page grew by 348 bytes.
| Revision 17 — 14:05, 15 Jul 2025 API_Aurora (talk) convert a hard-coded date to the house format 5,245 bytes ±0 | Revision 18 — 21:10, 10 Aug 2025 ArcuateArt (talk) add see also to the sister hormone 5,593 bytes +348 | ||
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| 32 | This is why the pharmacology does not simply amplify the physiology. The nausea that accompanies agonist therapy reflects area postrema engagement that endogenous secretion does not produce at comparable intensity, and the sustained reduction in food intake reflects continuous rather than meal-linked signalling. | 32 | This is why the pharmacology does not simply amplify the physiology. The nausea that accompanies agonist therapy reflects area postrema engagement that endogenous secretion does not produce at comparable intensity, and the sustained reduction in food intake reflects continuous rather than meal-linked signalling. |
| 33 | 33 | ||
| + | 34 | It is also why reduced intake, not increased expenditure, dominates the weight effect: energy expenditure falls with weight loss as it does with any caloric deficit, and no incretin agonist has been shown to raise it. The glucagon component of [[Retatrutide|triple agonists]] is the deliberate attempt to add an expenditure arm.{{r|schwartz2000}} | |
| + | 35 | ||
| 34 | == References == | 36 | == References == |
| 35 | {{reflist}} | 37 | {{reflist}} |